Gynae: menstrual cycle and menstrual disorders Flashcards

1
Q

Outline the pathophysiology of puberty

A
  • 8 yrs- GnRH release increases, so FSH and LH levels increases and stimulate oestrogen from ovaries
  • 9-11 yrs- thelarche (breast development) begins
  • 11-12 yrs- adrenarche (pubic hair growth)
  • 13 yrs- Menarche (periods irregular at first)
  • All finished by 16yrs old, average menarche age is decreasing
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2
Q

Outline the pathophysiology of menstruation

A
  • Day 1-4= menstruation, when endometrium is shed & myometrium contractions occur (painful)
  • Day 5-13= GnRH pulses from HPA-> LH+FSH release, stim follicular growth. The follicles produce oestradiol and inhibin that suppress FSH in a negative feedback loop so only one follicle matures. As oestradiol levels continue to rise, get +ve feedback and sharp LH rise (ovulate) and endometrium reforms
  • Day 14-28= luteal/secretory phase-follicle now corpus luteum, produce oestradiol & progesterone (peaks day 21) Induces secretory changes in endometrium. Towards end, corpus luteum starts to fail if no fertilised egg so no more progesterone & oestradiol. Endometrium breaks down.
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3
Q

What are the causes of irregular menstruation and intermenstrual bleeding?

A
  • Anovulatory cycles, especially in early & late reproductive years,
  • Pelvic pathology- fibroids, polyps, adenomyosis, ovarian cyst, chronic infection, malignancy
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4
Q

What is the management for irregular bleeding?

A

IUS or combined OCP if no anatomical cause found. Otherwise, treat cause

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5
Q

Define oligomenorrhoea

A

Infrequent periods (More than 35 days to 6 months between them)

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6
Q

Define primary and secondary amenorrhoea

A

Primary- Periods not started by age 16
Secondary- Periods stop for 6 or more months

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7
Q

Classification of causes of amenorrhoea/ oligomenorrhoea

A
  • Physiological- in pregnancy, after menopause and during lactation
  • Pathological- hypothalamus, pituitary, thyroid, adrenals, ovary, uterus, outflow tract
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8
Q

What are hypothalamic causes of amenorrhoea and their treatments?

A
  • Hypothalamic hypogonadism- reduced GnRH release, and thus low LH and FSH, due to anorexia nervosa or excessive exercise
  • Tumours- Rare, MRI to exclude
  • Treatment: need oestrogen replacement and progesterone for endometrial protection- use combined OCP or HRT
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9
Q

What the pituitary causes of amenorrhoea and their treatments?

A
  • Hyperprolactinaemia due to benign hyperplasia or adenomas (reduces GnRH release). May have neruo signs (bitemporal hemianopia, headache) - Treat with bromocriptine, cabergoline (DA agonists that inhibit prolactin release), or surgery
  • Sheehan’s syndrome- severe postpartum haemorrhage causes pituitary necrosis and hypopituitarism (So low FSH and LH release)
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10
Q

What are the ovarian causes of amenorrhoea?

A
  • PCOS
  • Premature menopause
  • Congenital
    • Turners syndrome (45 XO genotype)- short stature, poor 2dary sex characteristics, IQ ok
    • Gonadal dysgenesis- ovary imperfectly formed due to mosaic abnormalities of X chromosomes
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11
Q

What are the outflow tract problems causing amenorrhoea and their treatments?

A
  • Imperforate hymen/ transverse vaginal septum- block menstrual flow, it accumulates in vagina (haematocolpos) or uterus (haematometra) Treat surgically
  • Absent vagina with or without (Rokitansky’s syndrome) uterus
  • Cervical stenosis
  • Asherman’s syndrome
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12
Q

What is PCOS?

A

Syndrome associated with biochemical and/or clinical abnormalities.

  • Increased LH and androgens (particularly relative to FSH)
  • Physical traits: hirsutism, acne, weight gain, oligomenorrhoea and infertility.
  • Multiple small follicles on the ovary (PCO)

Rotterdam Criteria - Diagnosed if 2 out of 3

  • Polycystic ovarian morphology on US
  • Irregular periods >5 wks apart
  • Hirsutism (clinical/biochemical-high testosterone)

*Metabolic syndrome with 40-50% developing diabetes later in life; cardiovascular disease and endometrial and breast cancer are common.

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13
Q

What is the aetiology of PCOS?

A
  • Genetic-disordered LH production+ insulin resistance.
  • The combination of raised LH+insulin act on PCO give more androgen production and reduced steroid hormone binding globulin (SHBG). High intraovarian androgens lead to excess small ovarian follicles (disrupt folliculogenesis)+ irreg/absent ovulation. Environmental factors (weight) can modify phenotype
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14
Q

What investigations should you do for PCOS?

A

Bloods

  • Blood glucose, HBA1c and lipids, total testosterone (normal to mod raised), steroid binding globulin (normal to low), free androgen index (normal or elevated)
  • LH and FSH levels: increased in women with premature ovarian failure and decreased in hypogondotropic hypogonadism, prolactin (exclude prolactinoma), TSH, testosterone (exclude tumour),

USS - (transvaginal) look for PCO

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15
Q

What is the treatment for PCOS?

A

Lifestyle

  • Encourage exercise, weight loss, stop smoking

If fertility desired:

  • Clomiphene – blocks oestrogen receptors in the hypothalamus, increasing the release of the FSH and LH (“fools” the hypothalamus into believing there is no oestrogen and causes stimulation of follicles). Given at the start of the cycle. Use transvaginal US to assess ovarian response (if none, increase dose) –ve effects on endometrium, only use for 6 months. Rx of multiple pregnancies
  • Others include gonadotrophins (if clomiphene fails – stimulate FSH production), metformin ( clomiphene effect, treats hair), or laparoscopic ovarian diathermy.

If fertility not desired:

  • COCP usually regulates menstruation and prevents endometrial hyperplasia (need 3-4 bleeds a year to protect endometrium).
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